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sunitinib  (MedChemExpress)
95
MedChemExpress sunitinib
ER stress induces RCC development and resistance to <t>sunitinib.</t> (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.
Sunitinib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sunitinib (sutenetm  (Pfizer Inc)
90
Pfizer Inc sunitinib (sutenetm
ER stress induces RCC development and resistance to <t>sunitinib.</t> (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.
Sunitinib (Sutenetm, supplied by Pfizer Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sunitinib/sunitinib+sutent/nct06326346-1-1-3
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n desethyl sunitinib  (MedChemExpress)
94
MedChemExpress n desethyl sunitinib
ER stress induces RCC development and resistance to <t>sunitinib.</t> (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.
N Desethyl Sunitinib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sunitinib/N-Desethyl+Sunitinib/10__1016_slash_j__jphs__2026__07__002-36-2-7
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medium  (MedChemExpress)
95
MedChemExpress medium
ER stress induces RCC development and resistance to <t>sunitinib.</t> (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.
Medium, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sunitinib/Sunitinib/pm42332154-76-22-14
Average 95 stars, based on 1 article reviews
medium - by Bioz Stars, 2026-08
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sunitinib resistant 786o 786o r cells  (MedChemExpress)
95
MedChemExpress sunitinib resistant 786o 786o r cells
ER stress induces RCC development and resistance to <t>sunitinib.</t> (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.
Sunitinib Resistant 786o 786o R Cells, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sunitinib/Sunitinib/pm42322858-51-0-14
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sunitinib resistant 786o 786o r cells - by Bioz Stars, 2026-08
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tyrosine kinase inhibitor sunitinib  (Kamada)
86
Kamada tyrosine kinase inhibitor sunitinib
ER stress induces RCC development and resistance to <t>sunitinib.</t> (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.
Tyrosine Kinase Inhibitor Sunitinib, supplied by Kamada, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sunitinib/inhibitor+kinase+sunitinib+tyrosine/pm42128231-64-15-23
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tyrosine kinase inhibitor sunitinib - by Bioz Stars, 2026-08
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sunitinib  (Pfizer Inc)
86
Pfizer Inc sunitinib
ER stress induces RCC development and resistance to <t>sunitinib.</t> (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.
Sunitinib, supplied by Pfizer Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sunitinib/sunitinib/us12622937-628-116-117
Average 86 stars, based on 1 article reviews
sunitinib - by Bioz Stars, 2026-08
86/100 stars
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sutent  (Pfizer Inc)
86
Pfizer Inc sutent
ER stress induces RCC development and resistance to <t>sunitinib.</t> (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.
Sutent, supplied by Pfizer Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sunitinib/sutent/us12622983-94-16-18
Average 86 stars, based on 1 article reviews
sutent - by Bioz Stars, 2026-08
86/100 stars
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ER stress induces RCC development and resistance to sunitinib. (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.

Journal: Oncology Letters

Article Title: A genome-wide Mendelian randomization study focusing on endoplasmic reticulum stress reveals novel genetic markers for renal cell carcinoma

doi: 10.3892/ol.2026.15732

Figure Lengend Snippet: ER stress induces RCC development and resistance to sunitinib. (A) qPCR (left) and TEM (right) confirming ER stress induction in RCC development. In total, 3 cell line models were used: HK-2 (normal renal epithelial cells), 293T with adriamycin (nephropathy model) and 786-O (clear cell RCC). qPCR markers for ER stress included GRP78, PERK, IRE1α, ATF6 and CHOP. TEM scale bar, 500 nm scale. The levels of ER stress markers are higher in sunitinib resistant (B) 786-O and (C) Caki-1 cells. ER stress phenotype was verified by qPCR (left) and TEM (right, 500 nm scale). (D) Western blot analysis of ER stress markers (p-PERK, PERK, p-IRE1α, IRE1α, p-eIF2α, eIF2α, GRP78, CHOP and ATF6) in 786-O and Caki-1 cell lines with or without sunitinib resistance, showing activation of ER stress pathways. ACTB served as the loading control. Treatment with 4-PBA (ER stress inhibitor) was included as an experimental control. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001. ER, endoplasmic reticulum; TEM, transmission electron microscopy; RCC, renal cell carcinoma; qPCR, quantitative PCR; GRP78, glucose-regulated protein 78; PERK, protein kinase R-like endoplasmic reticulum kinase; IRE1α, inositol-requiring enzyme 1α; ATF6, activating transcription factor 6; CHOP, C/EBP homologous protein; ACTB, actin beta; p-, phosphorylated.

Article Snippet: Sunitinib-resistant cell lines were developed by exposing ccRCC cells to low doses of sunitinib (cat. no. SU 11248; MedChemExpress).

Techniques: Western Blot, Activation Assay, Control, Transmission Assay, Electron Microscopy, Real-time Polymerase Chain Reaction